Evasion of the complement system by Leishmania through the uptake of factor H, a complement regulatory protein

Acta Tropica ◽  
2021 ◽  
Vol 224 ◽  
pp. 106152
Author(s):  
Adalberto Alves Pereira Filho ◽  
Alexandre Alves de Sousa Nascimento ◽  
Natália Alvim Araújo Saab ◽  
Ricardo Toshio Fugiwara ◽  
Grasielle Caldas D’Ávila Pessoa ◽  
...  
Keyword(s):  
Complement System ◽  
Regulatory Protein ◽  
Factor H ◽  
Complement Regulatory Protein ◽  
The Complement System

scholarly journals Complement Regulatory Protein Factor H Is a Soluble Prion Receptor That Potentiates Peripheral Prion Pathogenesis

2017 ◽  
Vol 199 (11) ◽  
pp. 3821-3827 ◽  
Author(s):  
Sarah J. Kane ◽  
Taylor K. Farley ◽  
Elizabeth O. Gordon ◽  
Joshua Estep ◽  
Heather R. Bender ◽  
...  
Keyword(s):  
Regulatory Protein ◽  
Factor H ◽  
Complement Regulatory Protein ◽  
Protein Factor

scholarly journals Simple Method To Distinguish between Primary and Secondary C3 Deficiencies

2003 ◽  
Vol 10 (2) ◽  
pp. 216-220
Author(s):  
Marlene Pereira de Carvalho Florido ◽  
Patrícia Ferreira de Paula ◽  
Lourdes Isaac
Keyword(s):  
Human Serum ◽  
Complement System ◽  
Factor H ◽  
Normal Human Serum ◽  
Alternative Complement Pathway ◽  
Complement Pathway ◽  
Factor B ◽  
Alternative Complement ◽  
Normal Human ◽  
The Complement System

ABSTRACT Due to the increasing numbers of reported clinical cases of complement deficiency in medical centers, clinicians are now more aware of the role of the complement system in the protection against infections caused by microorganisms. Therefore, clinical laboratories are now prepared to perform a number of diagnostic tests of the complement system other than the standard 50% hemolytic component assay. Deficiencies of alternative complement pathway proteins are related to severe and recurrent infections; and the application of easy, reliable, and low-cost methods for their detection and distinction are always welcome, notably in developing countries. When activation of the alternative complement pathway is evaluated in hemolytic agarose plates, some but not all human sera cross-react to form a late linear lysis. Since the formation of this linear lysis is dependent on C3 and factor B, it is possible to use late linear lysis to routinely screen for the presence of deficiencies of alternative human complement pathway proteins such as factor B. Furthermore, since linear lysis is observed between normal human serum and primary C3-deficient serum but not between normal human serum and secondary C3-deficient serum caused by the lack of factor H or factor I, this assay may also be used to discriminate between primary and secondary C3 deficiencies.

MOLECULAR GENETIC CHARACTERISTICS OF COMPONENTS OF THE COMPLEMENT SYSTEM IN SEVERE ACNE

2021 ◽  
Vol 100 (2) ◽  
pp. 40-48
Author(s):  
A.G. Rumyantsev ◽  
◽  
A.G. Rumyantsev ◽  
O.M. Demina ◽  
◽  
...  
Keyword(s):  
Nucleotide Sequence ◽  
Complement System ◽  
Molecular Genetic ◽  
Factor H ◽  
Host Cells ◽  
Pathophysiological Mechanism ◽  
Genetic Characteristics ◽  
Severe Acne ◽  
C3 Gene ◽  
The Complement System

It has been shown that the inflammatory response in acne develops at the early subclinical stages of the disease, sometimes before the formation of comedones. It is known that an important component of the innate immune system is the complement system, which includes more than 60 components, including 9 basic proteins (C1-C9), a variety of activation products (C3a, C3b, iC3b, C3d and C3dg), regulatory and inhibitory molecules [factor H, fH-like protein 1 (FHL1), CR1 (CD35), C4b-binding protein (C4BP), C1inh and vitronectin], proteases and secreted enzymes (factor B, factor D, C3bBb and C4bC2b), as well as receptors for effector molecules [C3aR, C5aR, C5L2 and C1q receptor (C1qR)]. The compliment is the central part of innate immunity, which is the first line of protection against alien and altered host cells. The objectives of this study were to determine and analyze the variants of the nucleotide sequence of the genes of the complement system C1QA, C1S, C2, C3, C5, C6, C7, C8A, C8B, C8G, C9 in patients with severe acne. Materials and methods of research: To achieve the target a prospective open non-randomized one-center study was carried out in 2017–2020. Under our supervision in the clinical setting at the Department of Skin Diseases and Cosmetology of the Pirogov Russian National Research Medical University, there were 50 patients in the main group and 20 participants in the comparison group (70 people in total) (42/60% men and 28/40% women) aged 15 to 46 years (median – 22,1 years). Molecular genetic diagnostics was performed in all 70 patients of the main and control groups by the method of high-throughput DNA sequencing – next-generation sequencing (NGS). Results: when analyzing the nucleotide sequence variants of the complement system genes identified in our study, it is shown that the severe form of acne probably has an association (4 SNPs of the C8A gene, 1 SNPs of the C8B gene, 2 SNPs of the C1S gene, 3 SNPs of the C3 gene, 2 SNPs of the C9 gene, 1 SNPs of the C7 gene, 1 SNPs of the C6 gene, 1 SNPs of the C2 gene, 2 SNPs of the C5 gene, 2 SNPs of the C8G gene), 13 SNPs of the complement system genes in introns (1 SNPs of the C8A gene, 1 SNPs of the C8B gene, 2 SNPs of the C1S gene, 1 SNPs of the C3 gene, 1 SNPs of the C7 gene, 2 SNPs of the C6 gene, 4 SNPs of the C5 gene, 1 SNPs of C8G gene), 6 SNPs of the complement system genes (2 SNPs of the C8B gene: one SNPs each in the 3'UTR and 5'UTR zones; 3 SNPs of the C3 gene in the 5'UTR zone, 1 SNPs of the C7 gene in the 3'UTR zone). Two mutations of the frame shift of the C2 gene (frameshift deletion) and the C9 gene (rs748464075, frameshift insertion) seem to have a protective effect in the development of acne. Conclusion: the obtained variants of the nucleotide sequence of the genes of the complement system C1QA, C1S, C2, C3, C5, C6, C7, C8A, C8B, C8G, C9, apparently, are associated with the formation of severe acne and cause an imbalance of the components of the complement system. It can cause a defect in chemotactic and phagocytic reactions, and as a result a disturbance of the regulation of the inflammatory reaction with chronization of the skin process occures. Thus, results of studies carried out, revealed – for the first time – polymorphic loci of genes of components of the complement system, the imbalance of which is the pathophysiological mechanism of acne.

Arg127 of complement regulatory protein Factor H is important for its secretion from human fibroblasts

2009 ◽  
Vol 46 (14) ◽  
pp. 2869
Author(s):  
José Antonio Tavares Albuquerque ◽  
Dayseanne Araújo Falcão ◽  
Lourdes Isaac
Keyword(s):  
Human Fibroblasts ◽  
Regulatory Protein ◽  
Factor H ◽  
Complement Regulatory Protein ◽  
Protein Factor

Functional properties of the allotypes of mouse complement regulatory protein, factor H: Difference of compatibility of each allotype with human factor I

1993 ◽  
Vol 30 (9) ◽  
pp. 841-848 ◽  
Author(s):  
Okada Michiyo ◽  
Kojima Ayako ◽  
Takano Hiromi ◽  
Harada Yoshinobu ◽  
Nonaka Mayumi ◽  
...  
Keyword(s):  
Functional Properties ◽  
Human Factor ◽  
Regulatory Protein ◽  
Factor H ◽  
Complement Regulatory Protein ◽  
Factor I ◽  
Protein Factor

The interaction between the host's complement system and the poxviral complement regulatory protein determines the lethality of ectromelia infection

2008 ◽  
Vol 45 (16) ◽  
pp. 4113
Author(s):  
Elizabeth A. Moulton ◽  
Paula Bertram ◽  
Nanhai Chen ◽  
R. Mark L. Buller ◽  
John P. Atkinson
Keyword(s):  
Complement System ◽  
Regulatory Protein ◽  
Complement Regulatory Protein

Sequence analysis of a cDNA clone encoding the C-terminal end of human complement factor H

1987 ◽  
Vol 7 (3) ◽  
pp. 201-207 ◽  
Author(s):  
A. J. Day ◽  
J. Ripoche ◽  
A. Lyons ◽  
B. McIntosh ◽  
T. J. R. Harris ◽  
...  
Keyword(s):  
Amino Acids ◽  
Tertiary Structure ◽  
Regulatory Protein ◽  
Peptide Sequencing ◽  
Factor H ◽  
Cdna Libraries ◽  
Complement Factor ◽  
Protein Factor ◽  
The Complement System ◽  
Full Length Clone

Peptide sequencing of the complement system regulatory protein, factor H, permitted the synthesis of a mixed sequence oligonucleotide probe. Human liver cDNA libraries were screened and factor H-specific clones selected. No full-length clone was obtained, but the largest available clone, R2a, was found to encode the C-terminal 657 amino acids of factor H. The derived amino acid sequence consists of 10 contiguous internally homologous segments, each about 60 amino acids long. Sequences homologous to these are found in several other complement and non-complement proteins. Such sequences are likely to represent a particular type of tertiary structure subunit.

Inherited complement deficiencies

1984 ◽  
Vol 306 (1129) ◽  
pp. 419-430 ◽  
Keyword(s):  
Immune Complex ◽  
Complement System ◽  
Lupus Erythematosus ◽  
Alternative Pathway ◽  
Strong Association ◽  
Factor H ◽  
Complement Deficiency ◽  
Classical Pathway ◽  
The Complement System

Isolated genetic deficiencies of individual components of the complement system have been described in man for all the components of the classical pathway and the membrane attack complex as well as for Factor I, Factor H and properdin. It is only for Factor B and Factor D of the alternative pathway that homozygous deficiency states are not so far known. Complement deficiency states provide the most direct way of looking at the role of the complement system in vivo and emphasize the importance of complement in resistance to bacterial infection and in particular to infection with Neisseria . This association is not unexpected since in vitro studies have shown complement to be an efficient enhancer of phagocytosis and inflammation. The particularly frequent occurrence of neisserial infection may be ascribed to the ability of these organisms to survive in phagocytic cells so that the plasma cytolytic activity provided by complement is needed to kill them. On the other hand the strong association between complement deficiencies and immune-complex diseases - especially systemic lupus erythematosus — was unexpected and seems paradoxical in view of the large part played by complement in the pathogenesis of immune complex mediated tissue damage. The paradox can be explained in part by the necessity for an intact complement system in the solubilization and the proper handling of immune complexes. It is also likely that complement deficiency can allow the persistence of low virulence organisms that produce disease solely by an immune complex mechanism. Recently described deficiencies of complement receptors and their effects in vivo are described.

scholarly journals Distinct and Separable Roles of the Complement System in Factor H-Deficient Bone Marrow Chimeric Mice with Immune Complex Disease

2006 ◽  
Vol 17 (5) ◽  
pp. 1354-1361 ◽  
Author(s):  
Jessy J. Alexander ◽  
O.G.B. Aneziokoro ◽  
Anthony Chang ◽  
Bradley K. Hack ◽  
Adam Markaryan ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Immune Complex ◽  
Complement System ◽  
Complex Disease ◽  
Factor H ◽  
Immune Complex Disease ◽  
Chimeric Mice ◽  
The Complement System
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